T. Tavli et al., DIASTOLIC SPECTRUM OF LEFT-VENTRICULAR HYPERTROPHY - THE IMPACT OF ETIOLOGY AND CORONARY-ARTERY DISEASE ON DOPPLER TRANSMITRAL VELOCITY, Cardiology, 87(5), 1996, pp. 436-442
Diastolic Filling of hypertrophied left ventricles has frequently been
observed by Doppler methods. We hypothesized that filling characteris
tics in hypertrophy vary with etiology and concurrent ischemia. For pa
tients with hypertrophy, the left-ventricular ejection fraction was >0
.47 +/- 0.16, end-diastolic pressure was > 15 +/- 2 mm Hg, end-diastol
ic volume index was <96 +/- 12 ml/m(2) and left-ventricular mass index
was 127 +/- 7 g/m(2). Peak E (early) and peak A (late) diastolic velo
cities and E-wave deceleration time, respectively, were as follows (si
gnificant unless otherwise indicated): normal subjects (NS), 79 +/- 9
and 82 +/- 19 cm/s, and 151 +/- 7 ms; cardiomyopathic hypertrophy, 63
+/- 16, 83 +/- 15 (NS) and 193 +/- 63, aortic stenosis without coronar
y disease, 110 +/- 10, 128 +/- 12 and 158 +/- 22 (NS); aortic stenosis
with coronary disease, 57 +/- 12, 86 +/- 26 (NS) and 187 +/- 39; hype
rtension without coronary disease, 107 +/- 9, 128 +/- 9 and 143 +/- 22
(NS); hypertension with coronary disease, 58 +/- 12, 84 +/- 26 (NS) a
nd 189 +/- 29. Conclusions: Hypertrophied left ventricles filled with
two diastolic Doppler patterns: a relaxation abnormality with low peak
E and delayed deceleration in hypertrophic cardiomyopathy, and a comp
liance abnormality with tall peak E and normal deceleration in pressur
e overload hypertrophy. When coronary artery disease occurred with pre
ssure overload hypertrophy, impaired relaxation was the dominant patte
rn. Therefore, in addition to the known physiologic influences on dias
tolic filling, the etiology and presence of coronary artery disease mo
dulate the configuration of transmitral velocities into hypertrophied
ventricles.